Aspiration Pneumonia and Pneumonitis

Aspiration pneumonia (infection occurring from the exposure) results from the swallowing of colonized oropharyngeal contents into the lower respiratory tract with subsequent inflammation and infection. 

Aspiration pneumonitis (Mendelson's syndrome) is from exposure of sterile gastric contents into the lower respiratory tract. This results in a rapid chemical pneumonitis due to irritation of the pulmonary tissues from the acidic material. 

Approximately half of the healthy adults aspirate small amounts oropharyngeal secretions during sleep. Sterile pneumonitis and aspiration pneumonia are difficult to distinguish from one another, even with bronchial lavage. 

Risk Factors for Aspiration

• Reduced Consciousness (EtOH, Drugs, Procedural Sedation, GA)
• Neurologic (Stroke, Seizure, TBI, Dementia, Chronic Neurologic Conditions)
• Oropharyngeal (Poor oral hygiene, Intubation)
• GI (GERD, Esophageal dysmotility, Oral/NG Tube feeding)

About one third of those who aspirate have “silent aspiration” without evidence of cough or gagging. 

Pathophysiology 

• Inflammation (peaks in 4 to 6 hours) --> Increase capillary permeability 
• These reactions may manifest clinically as a cough, pleuritic chest pain, fever, and radiographic findings. 

Typical bacterial species involved in aspiration pneumonia

• S. pneumoniae
• S. aureus
• H. influenzae
• Enterobacteriaceae in community-acquired aspiration pneumonia.

Hospital Acquired Aspiration - P. aeruginosa and gram-negative organisms

Antibiotic therapy for aspiration pneumonia should include coverage for anaerobic organisms.

Presentation

The clinical symptoms of aspiration pneumonia include fever, dyspnea, and productive cough. Patients may show up tachycardia, tachypnea, rales.  Other symptoms of systemic infection in the elderly and debilitated may be present, including a change in mental status, lethargy, and nausea or vomiting.

Witnessed aspiration is a key feature in the diagnosis of aspiration pneumonitis or pneumonia. Typically those with noninfectious aspiration are younger, and the aspiration is witnessed. These patients will present giving a history of aspiration and coughing immediately afterward. 

“Silent aspirators” are typically older and have a chronic neurologic disorder and will present with a cough or fever or general malaise. Historical features that suggest silent aspiration include general debility, recurrent cough, hoarseness, or dysphagia. 


Diagnosis

• CXR usually shows unilateral focal or patchy consolidations in the dependent lung segments (Right lower lobe is the most common in upright aspiration) 
• CT Scan

Initial CXR if done too early in the course may not show any changes

http://www.svuhradiology.ie/case-study/aspiration-pneumonia/

Recumbent Aspiration typically involves posterior portions of the upper lobes and the upper portions of the lower lobes
Upright Aspiration typically involves the most dependent portions i.e. basal segments of the lower lobes. 

Treatment
Large volumes aspiration may require suctioning of the tracheobronchial tree or bronchoalveolar lavage to clear the airway. Bronchodilators aid aspiration-induced bronchospasm.

• Community-Acquired Aspiration (S. aureus, S. pneumoniae, and H. influenzae) - Use Co-Amoxiclav or Levofloxacin
• Suspected MRSA - Add Vancomycin or Linezolid
• Patients with severe periodontal disease, putrid sputum, or lung abscess - Give piperacillin-tazobactam. 

Clinically well-appearing patients with normal gas exchange are candidates for possible discharge with instructions to return if they experience worsening symptoms. Those with significant comorbidities need to get admitted for observation and Antibiotics. 

Further reading

1. Kikuchi R, Watabe N, Komino T, et al: High incidence of silent aspiration in elderly patients with community acquired pneumonia. Am J Respir Crit Care Med 150: 251, 1994. 
2. Marik PE: Aspiration pneumonitis and aspiration pneumonia. N Engl J Med 344: 665, 2001. 

Posted by:

              

     Lakshay Chanana

     

     ST4 Trainee

     Royal Infirmary of Edinburgh
     Department of Emergency Medicine

     Edinburgh
     Scotland

     @EMDidactic

Procedural Sedation in ED

Procedural Sedation and Analgesia (PSA) is the administration of sedatives and analgesics or dissociative anesthetics to induce a depressed level of consciousness while maintaining cardiorespiratory function so that a medical procedure can be performed with little or no patient reaction or memory. 

PSA Terminology and levels of Sedation

Minimal sedation (anxiolysis): A drug-induced state during which patients respond normally to verbal commands. Although cognitive function and coordination may be impaired, ventilatory and cardiovascular function is unaffected.

Moderate sedation (formerly conscious sedation): A drug-induced depression of consciousness during which patients respond purposefully to verbal commands, either alone or accompanied by light tactile stimulation. Reflex withdrawal from a painful stimulus is not considered a purposeful response. No interventions are required to maintain a patent airway, and spontaneous ventilation is adequate. Cardiovascular function is usually maintained.

Deep sedation: A drug-induced depression of consciousness during which patients cannot be easily aroused but respond purposefully after repeated or painful stimulation. The ability to independently maintain ventilatory function may be impaired. Patients may require assistance in maintaining a patent airway, and spontaneous ventilation may be inadequate. Cardiovascular function is usually maintained.

Dissociative sedation: A trancelike cataleptic state induced by the dissociative agent ketamine and characterized by profound analgesia and amnesia with retention of protective airway reflexes, spontaneous respirations, and cardiopulmonary stability.

General anesthesia: A drug-induced loss of consciousness during which patients cannot be aroused, even by painful stimulation. The ability to independently maintain ventilatory function is often impaired. Patients frequently need assistance in maintaining a patent airway, and positive pressure ventilation may be required because of depressed spontaneous ventilation or drug-induced depression of neuromuscular function. Cardio- vascular function may be impaired.

Evaluation before PSA

• ASA Grading
• Inspect Airway for difficulty (short neck, micrognathia, large tongue, trismus, morbid obesity, a history of difficult intubation, or anatomic anomalies of the airway and neck)
• Last Ate/Drank
• Systemic Disease (Most agents can cause vasodilatation and hypotension, particularly in patients with pre-existing hypovolemia)
• Medications
• Allergies
• Prior Sedation
• Estimated Weight 

PSA ideally needs 2 Doctors and 1 Nurse 

There is no evidence that the risk of aspiration during procedural sedation is increased with recent oral intake. Current guidelines regarding the safe fasting period prior to procedural sedation are based on expert consensus. Recent food intake is not an absolute contraindication. However, f the risk of aspiration is concerning, waiting 3 hours after the last oral intake before performing procedural sedation is associated with a low risk of aspiration, regardless of the level of sedation.

Equipment, Drugs and Preparation (Prepare as you do for Intubation)

• Suction/O2
• BMV
• OPA/NPA
• Laryngoscopes 
• ET Tube/Stylet
• Bougie
• LMA
• Defibrillator
• Difficult Airway Equipment 

Drugs

• Analgesics (Fentanyl/Morphine/Ketamine/NO)
• Sedatives (Propofol, Midazolam, Etomidate)
• Anti-emetics
• Reversal Agents
• IV Fluids

Monitoring during PSA

Type of monitoring and Number of Providers

Interactive monitoring i.e. direct observation of the patient to assess the depth of sedation and observe for hypoventilation or apnea, upper airway obstruction, laryngospasm, vomiting, or aspiration. 

Electronic monitoring i.e. using equipment to assess arterial oxygenation, ventilation, blood pressure, and cardiac rate and rhythm. Moderate and deep sedation require constant observation and continuous monitoring. 

• Consciousness level
• Resp Rate and Effort
• ECG
• Blood Pressure
• SpO2
• ETCO2

Pulse oximetry is not a substitute for monitoring ventilation, as hypoventilation or apnea develop before oxygen saturation decreases, especially in patients who receive supplemental oxygen.

Ventilation can be electronically monitored using capnography. The end-tidal carbon dioxide correlates with the arterial partial pressure of carbon dioxide so that an end-tidal carbon dioxide above 50 mm Hg (6.6kPa) or an increase in end-tidal carbon dioxide >10 mm Hg (1.33 kPa) indicates hypoventilation. A flat-line capnogram can be due to apnea, upper airway obstruction, or complete laryngospasm. Normalization of the waveform after chin lift, jaw thrust, or oral airway placement confirms that apnea was due to upper airway obstruction. Capnography during procedural sedation allows the early recognition of adverse events. Because the risk of respiratory depression increases with the depth of sedation, capnography should be considered for moderate sedation and is recommended for prolonged deep sedation.

Sequence of Events 
1. Give Analgesics (morphine/fentanyl) first. 

2. Preoxygenate: Supplemental oxygen reduces the incidence of hypoxemia and has no adverse clinical effects. In morbidly obese patients, BiPAP may be useful to facilitate adequate sedation while averting hypoventilation. Connect appropriate monitoring equipment to the patient.

3. Give Sedative Agent
Once administered, observe and monitor the patient until the peak effect of the initial sedative dose has been reached. Once the patient has achieved the target sedation level, do the procedure and give additional doses in small increments if needed. 

Complications

• Aspiration
• Hypoxia
• Hypotension
• Allergic Reaction
• Agitation
• Vomiting
• Delayed Recovery

Issues arise due to using an inappropriate agent or giving an incorrect dose or administering through a wrong route and poor use of adjunctive agents. Time of onset from injection to the initial observed effect must be appreciated bby the provider, especially when using drugs in combination, to avoid stacking of drug doses and oversedation.

Sample Discharge Instructions

Here is a full checklist for PSA done by @emupdates
RCEM ED Sedation Proforma 


Key Points

• Pulse oximetry measures the percentage of hemoglobin that is bound to oxygen and is not a substitute for monitoring ventilation because of the variable lag time between the onset of hypoventilation or apnea and a change in the oxygen saturation of hemoglobin molecules.
• The emotional state of a patient on induction strongly correlates with the degree of distress on emergence and in the days immediately after the procedure.
• There is no universally correct or preferred medication or drug regimen. Many options are acceptable and successful. The best choice is an agent whose pharmacologic properties are familiar to the operator and that is used frequently by the operator, is easily titratable, and has a short duration of action or is readily reversible. 
• Clinicians must have a thorough knowledge of the pharmacokinetics, dosing, administration, and potential complications of the PSA agents that they use. 

Posted by:

              

     Lakshay Chanana

     

     ST4 Trainee

     Royal Infirmary of Edinburgh
     Department of Emergency Medicine

     Edinburgh
     Scotland

     @EMDidactic

DNB Emergency Medicine (Diplomate of National Board )

Guest Post by Manasa Seshadri 

I gave my final DNB theory exam, in Emergency Medicine in June 2018. And I cleared the exam. We had 4 papers, spread over (crammed in) 3 days; second day with one paper in the morning, one in the evening. Each paper was for 100 marks, with 10 questions in each. 

The following is few points I had written , about things that helped me prepare for the theory exam and thank god, clearing it. Have edited it a little and sharing it now. I have written these points for my current field, Emergency Medicine. Parts of it will be helpful for all specialities. These are specific for DNB theory, I say that only because of lack of knowledge about how MD guys prepare, maybe quite similar, their question paper pattern differ from DNB though.

Please ask your seniors and others for advice. Their advice may differ from mine. Follow whatever you feel more comfortable with.

To pass an exam, you will need 6 months of preparation. That’s a minimum. Start now if you are late, start now if you are early.

BOOK : The only book I read was Tintinallis. I had planned to read some special books for paediatrics and trauma, but ended up not reading anything else because of the familiarity I had gained with Tintinallis and because I wasn’t sincere enough to make time for reading anything else. Your seniors may suggest other books for you. Please keep your options open as I haven’t seen any other book as of now, to offer an opinion.

If you are reading the book for pleasure, to understand the subject, to have fun while reading, do it before the last 6 months, because none of this pleasure reading will count when you are writing your paper 

Following is just for the last 6 months of reading:

CAN I OMIT ANYTHING? The answer I believe is, no.Read every line from the book. Including history and epidemiology – they asked us history of Nipah as a part of 10 mark question on Nipah(it was expected that we would be asked about Nipah, but history of the disease might have been something we wouldn’t have taken seriously) . I wouldn’t take the risk of omitting anything because it feels irrelevant or odd to be asked as a question. 

NOTES. I can’t stress the importance of making notes more. Make notes. Of everything you read. From any book / journal or paper you read. This notes will be the only material you should be reading during your revision. The revision you will be doing in the last 20 days/ 1 month or if you are sincere enough, last 2 months before exam! What you read in last 20 days is the only part you will remember when you are writing the paper.

Notes can be hand written (I prefer this method being an old fashioned person that I am) or typed (very satisfying for the OCD types and for those who know your way around the “bullets” and “changing list level” while using bullets in the word doc (I am not the one who is good at this and unfortunately I selected this method) Sounds nerdy, but helps knowing your type before you start. Notes should be pointers/ one liners or just 4 or 5 words in a line. That’s how you write your answers in the exams too. 

Notes will give you a perspective of what you have read, help you understand the chapter and help you prepare your answer for the exam, so that you need not spend any minute getting creative and spinning a story when you are writing the exam, and just write down the points you made.

“ENUMERATE “is a thing with DNB papers. “Enumerate causes of post-partum haemorrhage”, “enumerate the cold related injuries” etc. When you are starting the chapter, you can make a note of the main headings covered in that chapter in your notes or a stick-on, because that may just be your 2 or 3 marker. 2 marks seems less now. But when you are receive your question paper in your hand, it’s really a very big number!!

QUESTION PAPERS : You have to know the previous years’ question papers. They cover most topics from the text book, and when you know those topics, none of the questions will seem absurd or shocking to you. You will have 4 years papers in Emergency Medicine, including the June 2018 one, 4 papers each year. Each 10 mark question is subdivided into 2/3 and 4 markers, and each of them are specific, to the point questions. So very minimum scope for storytelling, be warned

If you are starting with question papers, finish the entire chapter from which that particular question has been asked. At the end of 4 papers including the recent June 2018 session, you will end up finishing 150 or more chapters of the total 303 chapters in Tintinallis book.

TABLES : you will know when you do the papers how many questions can be answered by knowing the tables and figures in the text book. 1 of those 3 or 4 sub- questions will invariably be a table from that chapter. Learning tables is near complete rote, so keep time to revise the tables again and again. And again. Your mnemonic habits from PG entrance exam preparation will be handy here.

REVISION : you need 3 months for revision, at least 2 months. And 3 times revision. They may say no, but most students from all departments revise atleast 3 times before final exam. Also, I am a slow learner. I am sure, there are people here, who need less time to read or revise, so decide for yourself how many months or how many times revision you need before exam. For a 6 month preparation period - If you are setting aside 3 months for revision, you have 3 months to finish first time reading. That’s 303 chapters in 90 days. That’s 3 chapters per day on an average. Luckily you have a lot of 3 and 4 pages small chapters in the book. Club them with 10 or 15 page chapters and read them. 

It’s ok if you don’t finish all 303 chapters in this first 3 months. Stretch your first time reading to 4 months and keep aside 2 months for revision. Keep track of the chapters you have never looked at (these are the moulds that you never felt comfortable looking at. Keep a separate track of chapters that you need more time to revise, that you need to refer from other sources . “Keeping track” may sound childish, but it helps you not feeling overwhelmed, and that’s a good thing when you are preparing for exam.

Study for a fixed number of hours in a day. 

Set aside those hours depending on your comfort, discipline, sleep wake cycles that you are habituated to. 

Exercise.

Watch movies.

Take short trips.

Enjoy studying. 

All the best.

Confession - I solemnly swear I didn't stick to the plan I enumerated above, wish I had though but sure as hell, I had planned it. Please do better than me. It will help.

Manasa Seshadri 

Diplomate of National Board (DNB) is a title awarded by the National Board of Examinations (NBE), an autonomous academic body under the Ministry of Health and Family Welfare, Government of India to candidates who successfully complete their postgraduate or postdoctoral medical education under it. DNB is recognised by the Government of India. Also, the Ministry of Health and Family Welfare has issued notification mentioning that DNB should always be considered equivalent to MD. 

Pulmonary Hypertension

Introduction

Pulmonary vascular system is a high-flow, low-resistance circuit. Normal pulmonary arterial systolic pressures range from 15 to 30 mm Hg, whereas diastolic pulmonary arterial pressures range from 4 to 12 mm Hg and Pulmonary hypertension is defined as a mean pulmonary arterial pressure >25 mm Hg at rest or >30 mm Hg during exertion.

Although echocardiography can estimate pulmonary arterial pressure in a patient with suspected pulmonary hypertension, definitive diagnosis requires right heart catheterization. The World Health Organization classifies pulmonary hypertension into five categories based on cause and response to treatment:

Accurate classification of pulmonary hypertension is key to directing treatments. Regardless of the cause, patients with pulmonary hypertension have high morbidity and mortality rates.

Pathophysiology

Endothelial dysfunction results in an imbalance between endogenous vasodilators and vasoconstrictors with net effect leading to vasoconstriction and formation of in situ thrombi. Other pathologic processes include alterations in microvascular permeability, abnormal hypoxic vasoconstriction, microvascular thrombosis, and the formation of plexiform lesions, leading to vascular remodeling. 

Ultimately, these abnormalities result in sustained elevations of pulmonary vascular resistance and impairment of pulmonary blood flow leading to RV dilatation and poor contractility. With progressive RV dilation, the intraventricular septum is displaced toward the left ventricle. This displacement inhibits left ventricular filling and ultimately impairs cardiac output and systemic perfusion.

Clinical Presentation 

• Symptoms can be non-specific which often leads to delayed diagnosis
• Dyspnea, fatigue, chest pain, near syncope, syncope, exertional lightheadedness
• Orthopnea, paroxysmal nocturnal dyspnea, and peripheral edema

The physical examination is often normal in the early stages of pulmonary hypertension.

Late signs include a holosystolic tricuspid regurgitation murmur, jugular venous distention, hepatomegaly, ascites, and lower extremity edema

Diagnosis 

ECG: The most common ECG abnormality seen in pulmonary hypertension patients is right axis deviation. Additional findings associated with pulmonary hypertension include an R/S ratio >1 in lead V1, an R/S ratio<1 in leads V5 and V6, a qR complex in lead V1, an S1Q3T3, right atrial enlargement in the inferior leads, and an incomplete or complete right bundle branch block. The most common dysrhythmias in patients with pulmonary hypertension are atrial fibrillation, atrial flutter, and atrioventricular nodal reentrant tachycardia.

B-type natriuretic peptide and N-terminal B-type natriuretic peptide are often elevated  Elevations in troponin from myocardial ischemia or a strain-induced leak can be seen.

CXR: Common abnormalities associated with pulmonary hypertension include enlargement of the right atrium, RV, and hilar pulmonary arteries. 

TTE: Transthoracic echocardiography is the best initial diagnostic test to assess pulmonary hypertension in the ED. It allows estimation of the pulmonary artery systolic pressure and detection of decreased RV function, right atrial hypertrophy right ventricular hypertrophy and leftward deviation of the intraventricular septum.

Treatment 

No consensus guidelines exist for the management of critically ill patients with pulmonary hypertension in the ED. The mainstays of ED therapy include:

1. Supplemental oxygen (Target SpO2 >90%)

2. Optimizing intravascular volume, augmenting right ventricular function, maintaining coronary artery perfusion, and decreasing right ventricular afterload 

Treatments caveats:

• Intubation: In patients with severe pulmonary hypertension, intubation and venti- lation can cause rapid cardiovascular collapse due to increased intrathoracic pressure from positive-pressure ventilation and effects of sedative medications on right ventricular function and systemic vascular resistance. Adjust the respiratory rate to avoid hypercapnia, which can increase pulmonary vascular resistance, pulmonary artery pres- sure, and RV strain.
• Fluids in RV Failure: Volume overload can cause RV dilation, displacing the intraventricular septum, impairing left ventricular output, and ultimately compromising tissue perfusion.3 For patients who are hypovolemic, give serial boluses of an isotonic crystalloid solution in 250- to 500-mL aliquots with close monitoring.
• RV Dysfunction: Dobutamine is preferred inotrope of choice. Avoid doses>10 micrograms/kg/min, because large doses can increase pulmonary vascular resistance and cause tachydysrhythmias and hypotension. For patients unable to tolerate dobutamine, milrinone is an alternative. Higher doses of milrinone can cause hypotension.
• RCA Perfusion: For the hypotensive pulmonary hypertension patient, use a vasopressor to increase aortic root pressure and maintain RCA perfusion. Norepinephrine is recommended for this purpose. Avoid high doses of nor- epinephrine because it can increase pulmonary vascular resistance and impair right ventricular output.
• RV Afterload reduction: These medications are rarely used in ED setting. Reducing right ventricular afterload with pulmonary vasodilators is a critical component in the management of stable patients with pulmo- nary hypertension. The most commonly used pulmonary vasodilators are prostanoids, endothelin receptor antagonists, and phosphodiesterase-5 (PDE-5) inhibitors. These medications are used primarily in the treatment of patients with pulmonary arterial hypertension. 

Prostanoids (epoprostenol, treprostinil, and iloprost) are potent vasodilators and are the initial treatment of choice in patients with pulmonary arterial hypertension and right ventricular failure. These medications have antiplatelet and antiproliferative properties.

Endothelin receptor antagonists (Currently not used for critically ill ED patients) are administered orally and increase exercise capacity, improve hemodynamics, and can delay the time to clinical worsening in pulmonary hypertension patients. Drugs: bosentan and ambrisentan. 

PDE-5 inhibitors (Currently not used for critically ill ED patients) sildenafil and tadalafil are approved for use in patients with pulmonary hypertension. They are administered orally, seeking to improve hemodynamics and exercise capacity in patients with pulmonary arterial hypertension.

Pulmonary HTN patients presenting to ED are often critically ill and require HDU/ICU level care. Therefore, almost all of them require admission with expert input. 

Posted by:

              

     Lakshay Chanana

     

     ST4 Trainee

     Royal Infirmary of Edinburgh
     Department of Emergency Medicine

     Edinburgh
     Scotland

     @EMDidactic